has homology to immunoglobulin and mucin-like adhesion receptors and to IgA1.
In specific, expression was moderate for [CD4.sup.+] and [CD8.sup.+] T-lymphocytes, while high for [CD68.sup.+] macrophages and MAdCAM-1. Tissue expression score was significantly higher (p < 0.001) in the group RFA compared to the group Sham for all biomarkers (Figure 1).
Receptors and their ligands necessary for T-cell homing in the intestine include MAdCAM-1, integrin a4b7, lymphocyte function-associated antigen-1, intercellular adhesion molecule-1, very late antigen-4 (a4b1), vascular cell adhesion protein 1, CCR9, CCL25, P-selectin glycoprotein ligand-1, and P-selectin .
According to animal studies, obstructive jaundice downregulates the numbers of [CD4.sup.+] and [CD8.sup.+] T-lymphocytes and MAdCAM-1 expression in the lamina propria .
Vedolizumab specifically binds to the alpha4beta7 integrin and blocks its interaction with MAdCAM-1
, therefore inhibiting the white blood cells from entering the inflamed gut tissue, thus decreasing inflammation.
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As the blockade of [alpha]4[beta]7 integrins prevents the adhesion of activated T lymphocytes to the mucosal addressin cell adhesion molecule 1 (MAdCAM-1
) and their extravasation into the gastrointestinal mucosa , natalizumab has been also approved for the treatment of moderate-to-severe CD in the USA .
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